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Sadaf Baig ppt

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Today We WillDefine hepatitis, viral hepatitis & the liverLearn about the 5 different types of viral hepatitis

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What Is Hepatitis?Hepatitis means inflammation of the liver ◦ Hepat (liver) + itis (inflammation)= HepatitisViral hepatitis means there is a specific virus that is causing your liver to inflame (swell or become larger than normal)

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The LiverIs located in the upper right quadrant of the abdomen •Cleans the blood •Regulates hormones •Helps with blood clotting •Produces bile •Produces important proteins •Maintains blood sugar levels •And much, much, more• The liver is essential for life !

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Inflammation Walls of scar tissue begin to Healthy liver cells form become trapped by a wall of scar tissue

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Hepatitis ACa used by hepatitis A virusCaHumans as their reservoirSOC: Infected feces, HAV-contaminated foodPOC: 1–2 weeks before the onset of symptoms until about 7 daysafter the patient becomes jaundiced.Fecal oral contaminationOral anal sexual activity contamination,shellfish from contaminated waterIncubation 18 – 45 daysImmune globulin within two weeks of exposure

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EtiologyHepatitis A virus (HAV) HAV is one kind of picornavirus and used to be classified as enterovirus type72, but recently, it is considered to be classified as heparnavirus Hepatitis A virion is a naked spherical particle, diameter 27nm Consists of a genome of linear, single-stranded RNA, 7.5kb. The genome may be divided into 3 coding region: P1 region (encoding structural protein), P2 and P3 regions (encoding non-structure protein) During acute stage of infection, HAV can be found in blood and feces of infected human and primates Marmoset and chimpanzee are susceptible animals

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Pathogenesis:Hepatitis A, EInoculation of the pathogen (entrance gate – small intestine).Viremia.Viral fixation on hepatocytes, intracellular localization.Primary replication of the virus.Excretion with a goal to intestine.Part of the viruses caused viremia (prodromal period of the disease).Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis.Immune response, elimination of the virus.

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Hepatitis ASIGNS AND SYMPTOMS •Most are anicteric and asymptomatic •Flu-like URTI with low-grade fever •Anorexia •Indigestion •nausea •Aversion to cigarette smoke and other strong odors •May or may not be jaundiced

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Hepatitis EHepatitis E Virus (HEV)Reservoir: Infected Humans and Animals: wild and domestic esp. swineIncubation: 14-60 daysPeriod of Communicability:-Not known.- Hepa-E virus has been detected in stools 14 days after theonset of jaundice and approximately 4 weeks after ingestion ofcontaminated food orwater and persists for about 2 weeks.Source of infection: - Contaminated water in areas of poor sanitation -household member,sex partners, shared injection equipment S/S: JAUNDICE is almost always present

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EpidemiologySource of infectionHepatitis A and E: patients with acute hepatitis and person with sublinical infectionRoute of transmissionHepatitis A and E: fecal-oral route predominantly

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Clinical pictureConvalescence stage: Signs & symptoms gradually disappear Jaundice may persist for some times due to affinity of bile pigment to elastic tissue Complete recovery of liver may take up to 6 months

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Susceptibility and immunity of population Hepatitis A Most adult has anti-HAV due to covert infection. Infant under 6 month acquired antibody from mother. Young children is susceptible Hepatitis E Common susceptible. Children appear covert infection, adult show overt infection

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Etiology Hepatitis B virus (HBV)HBV is a kind of hepadnovirusThree particles in serum: spherical particles and tubular particles with a diameter of 20 nm, composed of HBsAg large particles with a diameter of 42 nm, named Dane particle. It consists of an outer protein shell (envelope, contain HBsAg) and an inner body ( core, contain HBcAg, HBeAg, HBV- DNA and DNAP )

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EtiologyHBcAg—anti-HBc system HBcAg can be found in the nuclei of liver cells, no free HBcAg in serum HBcAg is the marker of replication of HBV The stage called window phase Anti-HBc IgM is a marker of acute infection and acute attack of chronic infection of HBV. Anti-HBc IgG is the marker of past infection, high titer means low level replication of HBV

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EtiologyHBSAg Related to chronocity, activity of hepatitis B or liver cancerResistance Resistant to heating and common disinfections. Chimpanzee is susceptible to HBV

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Hepatitis BHepatitis B Virus (HBV)Reservoir: HumansSource of infection: -infected individuals - receipt of blood transfusion orother blood products - use of shared needles - history of tattooing, ear or bodypiercing, or acupunctureIncubation: 30-180 daysPeriod of communicability:-1-2 months before and after the onset ofsymptomsMode of transmission: Heterosexualtransmission, contact with blood and bodyfluids

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Pathogenesis:Hepatitis BInoculation of the pathogen.Viremia.Viral integration and replication in hepatocytes, also may be in blood cells, bone marrow, lymph nodes, spleen.Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis.Immune response, elimination or persistence of the virus.

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Etiology Hepatitis C virus (HCV) HCV is a member of flavivirus family. HCV genome is a single stranded positive-sense RNA and contains 9.4kb The genome contains 5’-non coding region, C region, E region and NS region HCV genome may be divided into many types and subtypes. Resistance Antigen-antibody system The concentration of HCV in blood is low, HCV Ag has not be detected, anti-HCV is the indicator of infection and the marker of infectivity HCV-RNA HCV-RNA may be detected from blood or liver tissue, it’s the direct evidence of infectivity

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• Hepatitis C – Is similar to that of HB. CTL and some cytokines play an important action – The chronicity is related to the variability of gene – HCV infection is related to HCC closely but HCV does not integrate to liver cells, so from HCV infection to HCC may be related to chronic inflammation and cirrhosis

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Hepatitis DHepatitis D Virus (HDV)Reservoir: humans Animals: chimpanzee and pigsSource of infection: same as Hepa-BIncubation: 30-180 daysPeriod of communicability: not been yet determined,but virus excretion in stool has been demonstrated up to 14days after onset of illnessCo-infects with hepatitis B, close personal contact